Joel S. Bennett is at the Hematology-Oncology Division, Department of Medicine, University of Pennsylvania School of Medicine, Stellar-Chance Laboratories, Philadelphia, PA 19014, USA.
Trends Cardiovasc Med. 1996 Jan;6(1):31-6. doi: 10.1016/1050-1738(95)00126-3.
Glycoprotein IIb-IIIa (GPIIb-IIIa), a calcium-dependent heterodimer whose expression is restricted to platelets and megakaryocytes, contains a binding site for protein ligands such as fibrinogen and von Willebrand factor (vWf) whose exposure by platelet stimulation is a prerequisite for platelet aggregation. GPIIb-IIIa heterodimers are assembled from nascent GPIIb and GPIIIa subunits in the calcium-rich environment of the endoplasmic reticulum, and correctly folded heterodimers are transported from the endoplasmic reticulum through the Golgi apparatus to the cell surface. Agonist stimulation of platelets produces a conformational change in GPIIb-IIIa that exposes its ligand binding site, a process termed "insideout" signaling. This signaling process, by interacting with the cytoplasmic extensions of GPIIb and GPIIIa, converts the heterodimer from an inactive to an activated state capable of binding soluble ligands.
糖蛋白 IIb-IIIa（GPIIb-IIIa）是一种钙依赖性异二聚体，其表达仅限于血小板和巨核细胞，包含一个结合位点，用于结合纤维蛋白原和 von Willebrand 因子（vWf）等蛋白配体，血小板刺激后这些配体的暴露是血小板聚集的先决条件。GPIIb-IIIa 异二聚体由内质网中富含钙的环境中的新生 GPIIb 和 GPIIIa 亚基组装而成，正确折叠的异二聚体从内质网通过高尔基体运输到细胞表面。血小板激动剂刺激导致 GPIIb-IIIa 构象发生变化，暴露出其配体结合位点，这一过程称为“内向外”信号转导。该信号转导过程通过与 GPIIb 和 GPIIIa 的胞质延伸相互作用，将异二聚体从无活性状态转变为激活状态，从而能够结合可溶性配体。
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